Stereotypical Victims: Visibility of #MeToo Disclosures on Twitter.

The #MeToo movement has brought greater visibility to the topic of sexual assault in public discourse. We analyzed a dataset of 1,070 Twitter #MeToo self-disclosures to examine the relationship between online visibility (retweets and favorites) and the content of victim-survivors' self-disclosures such as victim's gender, relationship to the perpetrator, and the emotions expressed in the tweet. The visibility of sexual assault self-disclosures was shaped by the extent to which they align with stereotypical misconceptions of victimization.

Apolipoprotein E epsilon 4 is associated with the presence and earlier onset of hemorrhage in cerebral amyloid angiopathy.

Background And Purpose: Cerebral amyloid angiopathy is an important cause of intracerebral hemorrhage in the elderly. The epsilon 4 allele of the apolipoprotein E gene, recently established as a genetic risk for Alzheimer's disease, has also been suggested as a possible risk factor for cerebral amyloid angiopathy. We sought to determine whether this allele is specifically associated with hemorrhages related to amyloid angiopathy and whether it correlates with the age at which first amyloid angiopathy-related hemorrhage occurs.

Positive feedback in hypogonadal female mice with preoptic area brain transplants.

When fetal preoptic area (POA) brain grafts that contain gonadotropin-releasing hormone cells are transplanted into the third ventricle of adult female hypogonadal mice, the animals respond with sexual maturation, persistent estrus, and the ability to ovulate reflexively after mating. However, the absence of normal spontaneous ovulatory cyclicity suggests an impairment in positive feedback. We, therefore, studied the effect of administration of progesterone alone or of sequential estradiol benzoate and progesterone on plasma levels of luteinizing hormone (LH) in groups of hypogonadal (HPG) mice in persistent estrus after receiving POA grafts (HPG/POA).

Thymocyte maturity in male and female hypogonadal mice and the effect of preoptic area brain grafts.

Hypogonadal mice with a genetic deficiency of gonadotropin-releasing hormone (GnRH) have low levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and gonadal steroids. In this study we found differences from normal mice in many aspects of thymic development. Thymus weights and cellularity were higher in hypogonadal than in normal male mice but lower in hypogonadal than in normal females.

Transplanted gonadotropin-releasing hormone neurons promote pulsatile luteinizing hormone secretion in congenitally hypogonadal (hpg) male mice.

Congenitally hypogonadal (hpg) male mice are unable to synthesize biologically active gonadotropin-releasing hormone (GnRH). Implantation of normal fetal preoptic area tissue containing GnRH neurons into the third ventricle of adult hpg males significantly elevates pituitary levels of luteinizing hormone (LH) and corrects their hypogonadism. In all responding animals, immunoreactive GnRH neurons within the transplant innervate the median eminence of the host.

Quantitative analysis of synaptic input to gonadotropin-releasing hormone neurons in normal mice and hpg mice with preoptic area grafts.

Mutant hypogonadal (hpg) mice with a truncated gene for the precursor to gonadotropin-releasing hormone (GnRH) show certain aspects of recovery of reproductive function after receiving grafts of normal preoptic area into the third ventricle. We have previously shown that GnRH neurons from within the grafts can innervate the appropriate neural-hemal target in the host. To determine if in turn these exogenously derived neurons receive a synaptic input comparable to the GnRH neurons in the normal animal we have now carried out a quantitative ultrastructural analysis to compare the synaptic input to GnRH neurons in the normal preoptic area and in the grafts.

Plasma LH rises rapidly following mating in hypogonadal female mice with preoptic area (POA) brain grafts.

Hypogonadal female mice, genetically deficient in gonadotropin releasing hormone (GnRH), respond to preoptic area (POA) grafts obtained from normal fetal or neonatal mice with increased gonadotropin levels, ovarian and uterine development and continual vaginal estrus rather than spontaneous ovulatory cyclicity. Previous studies showed that such mice became pregnant following one overnight pairing with a normal male, indicating reflex ovulation. The present study evaluated plasma LH concentrations in relation to mating.

Accessory olfactory bulb transplants correct hypogonadism in mutant mice.

Transplantation of normal fetal gonadotropin-releasing hormone (GnRH) neurons from the accessory olfactory bulb (AOB) to the third ventricle of GnRH-deficient adult mutant mice reverses the genetically determined reduction in pituitary hormones and poorly developed gonads. The transplanted heterotopic AOB neurons adapt their morphology and secretory functions to what is observed with preoptic GnRH neurons when transplanted into deficient mice and in the normal intact mature animal. This suggests the presence of median eminence trophic factors affecting the growth, terminal sprouting, and functional behavior of the transplanted neurons.

Implantation of fetal preoptic area into the lateral ventricle of adult hypogonadal mutant mice: the pattern of gonadotropin-releasing hormone axonal outgrowth into the host brain.

Transplantation of fetal preoptic area tissue containing gonadotropin-releasing hormone neurons into the third ventricle of male hypogonadal mice resulted in an elevation of pituitary gonadotropin levels and correction of hypogonadism. This reversal of the neuroendocrine deficit was correlated with innervation of the median eminence by gonadotropin-releasing hormone axons. The specificity of fiber outgrowth suggested that local neuromodulatory factors might guide these axons to the nearby median eminence.

Female sexual behavior in hypogonadal mice with GnRH-containing brain grafts.

Hypogonadal female mice respond to GnRH-containing fetal preoptic area (POA) implants in the third ventricle with vaginal opening and persistent vaginal estrus, ovarian, and uterine development and increased gonadotropin secretion. When these females are mated with normal males, reflex ovulation results in pregnancy. In the present study, POA implants derived from neonatal pups, whether male or female, were also capable of supporting reproductive development in the hypogonadal female mice.

The effects of the age of intracerebroventricular grafts of normal preoptic area tissue upon pituitary and gonadal function in hypogonadal (HPG) mice.

Hypogonadal mice are deficient in the hypothalamic gonadotrophic hormone releasing hormone and as a consequence postnatal testicular development does not occur. Grafting preoptic area tissue from normal mice directly into the hypogonadal third ventricle dramatically reverses the hypogonadism; however, the age of the grafted preoptic area tissue is crucial to the survival and function of the graft. Grafting embryonic tissue (E16-18) resulted in 69% of the hypogonadal mice increasing testis weight some sevenfold within 30 days (5.

Ultrastructure of gonadotropin-releasing hormone neuronal structures derived from normal fetal preoptic area and transplanted into hypogonadal mutant (hpg) mice.

The hpg mutant mouse lacks the neurohormone gonadotropin-releasing hormone (GnRH) and hence has a reproductive deficit. This deficit can be corrected by placement of normal fetal preoptic area into the third ventricle (see Krieger et al., 1985).

Implantation of normal fetal preoptic area into hypogonadal mutant mice: temporal relationships of the growth of gonadotropin-releasing hormone neurons and the development of the pituitary/testicular axis.

Central nervous system tissue which included the preoptic area (an area rich in gonadotropin-releasing hormone neurons) was taken from normal 17-day fetal mice and transplanted into the infundibular recess of the third ventricle of the hypothalamus of 90-day male mutant hypogonadal mouse hosts that are unable to synthesize the neurohormone, gonadotropin-releasing hormone. The growth and development of gonadotropin-releasing hormone neurons and fibers in the donor and host tissue as well as recovery of the pituitary-testicular axis were followed from 10 to 120 days post-implantation. Testicular growth was evident in 94% of the hypogonadal animals within 30 days post-implantation, continued for 90 days but showed no further increase during the remainder of the experiment.